Melnik B, Plewig G
Hautklinik, Heinrich-Heine-Universität Düsseldorf.
Hautarzt. 1989 Nov;40(11):685-92.
The hypothesis proposed for the pathogenesis of atopy links the well-known alterations in cell-mediated and humoral immunity, the disturbances of mediator metabolism and the increased disposition of atopic epidermis for inflammation to a common underlying deficiency in the production of prostaglandin E1. The PGE1 deficiency is explained as the result of reduced delta-6-desaturase activity in atopic patients. The development of depressed cell-mediated immunity is regarded as a PGE1-dependent T-cell-maturation defect of the newborn's immune system post partum. Our hypothesis offers a novel approach to the prevention of atopy by administration of gamma-linolenic acid to newborns with increased risk of atopy and to nursing atopic mothers. Furthermore, it provides an explanation for the beneficial therapeutic effects of dietary supplementation of gamma-linolenic acid in patients with atopic dermatitis.
为特应性发病机制提出的假说将细胞介导免疫和体液免疫中众所周知的改变、介质代谢紊乱以及特应性表皮对炎症增加的易感性与前列腺素E1产生的共同潜在缺陷联系起来。前列腺素E1缺乏被解释为特应性患者中δ-6-去饱和酶活性降低的结果。细胞介导免疫抑制的发展被认为是产后新生儿免疫系统中依赖前列腺素E1的T细胞成熟缺陷。我们的假说为通过向有特应性风险增加的新生儿和患特应性的哺乳期母亲给予γ-亚麻酸来预防特应性提供了一种新方法。此外，它还解释了膳食补充γ-亚麻酸对特应性皮炎患者的有益治疗效果。
